Blood gas measurements in DKA: Are we searching for a unicorn?

Introduction

Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful.

It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation?

Diagnosis of DKA: Blood gas doesn’t help

These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate.

Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis.

Management: Does the pH help?

It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001).

A question often arises regarding whether bicarbonate should be used for patients with severe acidemia. There is no evidence to support for this practice, which may be harmful (British Guidelines)(1). For profoundly acidemic patients, my approach is occasionally to intensify the treatment of the DKA: give more fluid, more dextrose, and increase the rate of the insulin infusion (2). This makes more sense to me, because sicker patients may be more insulin-resistant. However, there isn't evidence to support this approach either. Overall, it's possible that the best approach would be simply not to check the pH.

Suppose that you would like to know the severity of the acidemia, perhaps to determine patient disposition (e.g. ward vs. ICU)? pH correlates fairly well with the serum bicarbonate. Thus, as discussed above, the serum bicarbonate can be used as a convenient index of acidosis severity.

Management: Does the pCO2 help?

Metabolic acidosis should induce a compensatory respiratory alkalosis (hyperventilation). In severe DKA, there may be concern that the patient will tire out and lose the ability to hyperventilate. Such fatigue would lead to profound acidemia.0

The most useful piece of information contained in a blood gas is probably the pCO2, which shows how well ventilation is compensating for the metabolic acidosis. This might theoretically allow detection of patients with inadequate respiratory compensation, who might theoretically benefit from ventilatory support. Realistically, how much will pCO2 affect management? This hinges entirely on the management strategy for supporting ventilation in DKA.

Management strategy for ventilatory support in DKA

Admitting that this is a data-free zone, high-flow nasal cannula (HFNC) is usually my preferred approach to noninvasive support in DKA (3). HFNC may reduce the work of breathing by decreasing the respiratory dead space and thereby improving the efficiency of ventilation. This may be a reasonable option in patients with severe acidosis (e.g. bicarbonate <10 mEq/L) when there is a concern that the patient may develop diaphragmatic fatigue over time.

When in doubt about whether the patient should receive HFNC vs. no support, there is little to be lost from a trial of HFNC. Patients who are struggling may feel better with the HFNC, whereas patients who don’t really need the support may be irritated by it.

It is generally wise to avoid intubation in DKA if possible. Otherwise, the decision to intubate in DKA is similar to the decision to intubate in general. This is primarily a clinical decision based on physical examination, clinical scenario, and anticipated course. Patients usually require intubation for issues other than the DKA itself (e.g. airway protection prior to emergent surgery).

Checking VBGs: Searching for a unicorn?

Above is my general approach to determining the appropriate level of ventilatory support (4). Usually a VBG is unnecessary. The only real utility of a VBG would be detection of occult ventilatory failure (referred to here as a unicorn). Specifically, a “unicorn” would be a patient who:

Despite years of searching I haven't yet found a unicorn. The closest I've come were a few patients who received opioids for abdominal pain, which blunted their compensatory respiratory alkalosis (creating a scary blood gas, but they were fine). Nevertheless, I plan to continue to search for unicorns by using VBGs in selected patients when there is a concern that intubation may be needed.

Rock Bottom Principle of DKA: Even if checking the pCO2does alter management, this is unlikely to improve the outcome

It is currently impossible to know whether checking pCO2 improves outcomes in DKA. The data simply doesn't exist. We can search for patients whose pCO2 is higher than we would like, and attempt to decrease their pCO2 with various modes of ventilatory support. Are we improving these patients' outcomes, or would they recover regardless of ventilatory support?

In general DKA patients almost always improve with appropriate treatment, often rapidly. Thus, nearly all patients will be their sickest (rock bottom) upon arrival. This means that if the patient is initially clinically OK and an abnormality in the VBG is “missed,” it probably doesn't matter. Within hours they will very likely be doing better and their blood gas will have improved (5).

This is not intended to belittle the value of careful clinical monitoring (e.g. trends in vital signs, examination, and chemistry panel). Occasionally underlying conditions may be missed or patients may require more aggressive therapy to improve. The key is probably the clinicaltrajectory: whether the patient is improving is more important than any particular VBG.

Evidence: Is blood gas analysis beneficial?

.This was a prospective observational study involving 195 patients with suspected DKA (based on hyperglycemia, ketonuria, and clinical features). Treating physicians wrote down their management and disposition plans without knowing the ABG results. Changes based on the ABG were as follows:

Knowing the ABG altered the diagnosis in two cases. However, in no case did the ABG affect the diagnosis of whether or not the patient had DKA. Note that an ABG shouldn't be needed to make a diagnosis of pneumonia: history, physical exam, pulse oximetry, chest radiography, and thoracic ultrasonography are likely more helpful.

In five cases, unexpectedly low or high pH affected the intensity of insulin therapy or disposition. However, this same information was actually contained in the bicarbonate concentration: patients with “unexpectedly low” pH had severe metabolic acidosis (bicarbonate <10 mEq/L) whereas patients with “unexpectedly high” pH had mild metabolic acidosis (bicarbonate >18 mEq/L). Thus, greater attention to the bicarbonate concentration may substitute for the pH.

In only one DKA patient did an ABG lead to changes in respiratory therapy (borderline hypoxemia with pO2 of 62mm prompted initiation of supplemental oxygen). A second patient was found to be hypercapneic due to obesity hypoventilation syndrome, but notably this patient did not actually have DKA.

Overall, in this series of 195 patients with suspected DKA (of whom 48 had DKA), routine ABG had a very little impact on patient management. ABG added little information that would not have been available from thoughtful evaluation including serum chemistries, history and physical examination, and additional tests as clinically warranted (e.g. chest X-ray, thoracic ultrasonography).

Hutten-Cazpski 2013, Can J Rural Med: How can you manage DKA without an ABG?

This letter describes one physician's transition from a teaching hospital to a small rural hospital without an ABG analyzer. Initially he was upset, but he quickly realized that he could manage just fine without blood gas analysis. Although blood gas analysis has been widely accepted in medicine, there is little evidence that it improves outcomes. It is often possible to manage patients based on their clinical examination instead of their ABG: might this actually improve care?

Perhaps experience taught me to pay better attention to the respiratory rate, urinary ketones, or the gestalt of how the patient looked, and I became a better doctor for it.

Don't be an ABG wanker

In honor of the late Dr. John Hinds, an ABG wanker is someone who focuses excessively on the blood gas, often while ignoring the patient or common sense. For example, an ABG wanker might order q2hr ABGs for a DKA patient to monitor their respiratory status, rather than looking in on them occasionally to examine them and ask how they feel (6). Delaying clearly necessary interventions such as transfer or intubation to obtain an ABG is another common offense. Although ABG wankers are primarily fixated in ABGs, a similar phenomenon can occur with VBGs.

Guidelines recommend checking an ABG or VBG in all patients with DKA. This practice is not evidence-based and should be abandoned.

ABG or VBG provides little information about whether or not the patient has DKA (beyond what is already known from the serum chemistries).

Rather than pH, serum bicarbonate may be used to gauge the severity of acidosis.

There is no evidence that detecting or reacting to a very low pH is helpful.

Decisions about the level of ventilatory support that a patient needs can almost always be made on a clinical basis. When in doubt, close attention to the patient with serial examination is often a sound approach. Focus on the patient, not the blood gas.

VBG might be helpful in cases where it is unclear whether the patient requires intubation, or if there is a significant underlying respiratory disease (e.g. COPD or obesity hypoventilation syndrome)..

Notes

I have previously recommended the use of isotonic bicarbonate towards the end of a DKA resuscitation, with a goal of gently correcting a residual non-anion-gap metabolic acidosis if one is present. This is explained further here (pearl #2). This practice should not be confused with the use of bicarbonate as the response to a scary low pH in the beginning of a DKA resuscitation, with a goal of somehow masking an anion-gap metabolic acidosis.

Volume depletion will cause the body to compensate by producing cortisol and catecholamines, which in turn reduce the sensitivity to insulin. Thus, allowing a patient to remain under-resuscitated may delay their recovery from DKA. These patients often have severe volume depletion and might benefit from aggressive goal-directed therapy (e.g. volume resuscitation until the IVC is reasonably full on ultrasonography). With regards to insulin therapy, there isn't anything magical about 0.1 mg/kg/hr of insulin infusion – perhaps a patient with profound acidosis would benefit from a higher rate? Overall, instead of blindly administering bicarbonate it may be better to think hard about the patient, what might be driving their DKA, and how their DKA management can be optimized.

Why use HFNC and not BiPAP? There is no evidence to support the use of either in DKA. BiPAP is fine, particularly in a patient with underlying COPD. My preference is usually HFNC for two reasons. First, patients often have diabetic gastroparesis and/or gastroenteritis and may be at increased risk of vomiting, a concern with BiPAP. Second, it may be harder to access the patient’s respiratory and neurologic status with BiPAP on.

Please note that this is purely a management algorithm. A patient with dyspnea may also merit diagnostic evaluation with a chest radiograph, ultrasound, etc.

There are some noteworthy exceptions to the rock bottom principle. First, if the DKA is due to a rapidly progressive underlying problem (e.g. septic shock), deterioration could occur despite perfect management. The second, and by far the most common exception, is resuscitation with large volumes of normal saline. If a patient presents with severe acidemia, bolusing them with several liters of normal saline will worsen their acidemia. Resuscitation with a balanced crystalloid should avoid this problem.

In the spirit of full disclosure, I have done similarly foolish things during my training. Thus, I do not believe that being an ABG wanker is necessarily a permanent character flaw, but instead it can be a temporary phase that many practitioners pass through as they grow (eventually, after obtaining lots of ABGs, it becomes clear when they are actually useful).

Share this:

25

Comment Here

Role

14Comment threads

11Thread replies

0Followers

Most reacted comment

Hottest comment thread

12Comment authors

Recent comment authors

Role

newestoldestmost voted

Guest

Mathias Tschopp

The blood gas (venous or arterial) has the distinct advantage of giving you a HCO3 value in 5 minutes, when it would take about an hour in most shops to get the result from a chem. blood work. That’s the main benefit I can see as having the diagnosis of the severity of the DKA in 5 minutes goes a great way towards patient orientation and treatment.

Although hypokalemia is uncommon in DKA, it does occasionally occur. Starting insulin prior to knowing the potassium could be problematic if the patient has pre-existing hypokalemia, as the insulin infusion could cause it to drop dangerously. For example, ADA guidelines recommend holding insulin if the potassium is <3.3 until potassium is repleted.

Therefore, I would generally not start treatment for DKA without a chemistry panel to prove the dx and determine the potassium. This could be run off of an iSTAT (or other point-of-care system) with a turn-around time of a few minutes if one is available.

Ultimately, I think the treatment is driven primarily by the chemistry panel rather than the blood gas.

That being said, there's nothing wrong with drawing venous blood, sending it to the lab for chemistries and also taking a bit extra for a VBG.

Yeah I really don’t understand the resistance to bedside VBG. Do you manage DKA with no venous blood samples at all? I would use a point of care bicarbonate and be thankful for the Hb, chloride, sodium, potassium, lactate, pCO2 and pH all within 2 minutes. I know DKA is often routine but patients are clearly allowed to present with more than one problem.

Are you suggesting that we should only use urinary ketones and RR to make decisions re disposition, need for ongoing insulin, potassium replacement and establishing the underlying cause?

Please tell me if I’m missing something but this all feels like a lot of effort to avoid a point of care VBG in a patient who you would otherwise wait 1-2 hours for results on.

I agree that your point-of-care panel with chemistries sounds like a great way to go.

I’m suggesting that management can be based solely on the chemistry panel (i.e. Na, K, bicarb, chloride), without a need for VBG or ABG (i.e. no pH or PaCO2). The chemistry panel is sufficient to guide potassium repletion, determine the anion gap, severity of the acidosis, and presence of any non-anion-gap acidosis that may be present.

It sounds like you are using a point-of-care system that gives you VBG and electrolytes simultaneously, in which case this is a non-issue for you. This issue is more relevant in a system where the VBG and chemistries need to be analyzed separately (e.g. two tubes sent to the lab, one on ice). Or in a situation where chemistries come back and the physician orders a separate draw for VBG or ABG.

Vote Up0Vote Down Reply

3 years ago

Guest

Juan Rivera

My POC system analyzes a full panel of electrolytes, do you think the lab’s chem profile is superior to that of a GEM 4000 blood gas machine? Do you have any reservations of using the blood gas machine’s electrolyte panel q2hrs or are you still consider a wanker if you do. 🙂

Thanks,

Juan J Rivera, RRT

Vote Up0Vote Down Reply

2 years ago

Guest

Joshua Michael

Good discussion. I would turn this around. Patient arrives sick. POC VBG and glucose back in two minutes. I would not wait 40 min for bicarbonate to begin treatment, and wouldn’t avoid ordering a VBG in lieu of a bicarb. So what’s the value of bicarb in terms of guiding initial therapy?

See my reply to the first comment above. Ideally would like to see a potassium value before starting insulin, so checking a VBG by itself won’t necessarily speed up therapy.

Vote Up0Vote Down Reply

3 years ago

Guest

Derek Louey

My take on this 1) Unless you suspect a mixed acid-base disorder (unicorn) or an alternative diagnosis to DKA, the additional data on VGG e.g. pH and pCO2 probably does not add much to the initial diagnosis 2) Once DKA is confirmed, monitoring with serum bicarbonate probably is enough to titrate insulin therapy (along with other clinical parameters) 3) The main aim is to observe ketosis resolving and acidosis improving (not glucose normalising) 4) The lab turnaround time for serum bicarbonate probably is not adequate for monitoring a sick DKA. Hence, the use of a bedside blood gas analyser (but as mentioned the pH and pCO2 is often redundant) 5) There is one added advantage of most analysers is that lactate, electrolytes and anion gap are also rapidly given. The may ask assist in revealing underlying circulatory compromise, titrating sodium and potassium replacement and determining the role of bicarbonate replacement An additional note, my practise (with absolutely no evidence based and only on pathophysiological reasoning) has changed over time I have tend to be much gentler nowadays with fluid and insulin to minimise rapid fluid shifts and the potential risk of cerebral oedema. Therefore, I will bolus fluid to stabilise… Read more »

Definitely. As discussed in some of the comments above, if you have a point-of-care analyzer which gives you everything simultaneously, then that’s a great way to go. A lot of this boils down to logistics and how tests are run in your shop.

Vote Up0Vote Down Reply

3 years ago

Guest

Craig Rosebrock MD

Loved the above comments … just have a few thoughts Do we need a blood gas? ever… well that is open for debate. I think we have to understand our roots a bit more. The use of blood gas analysis was never intended for DKA management. Our reliance on technology is a product of having said technology and using it to help make an informed analysis of the data and forming a plan. I am going to link two articles about the history of ABG’s and it may be a fun read. We get to see where our practice comes from and why it has evolved into what we do today. We use blood gas analysis in a lot of various disease states…most of which we dont NEED the gas but may benefit from a bit of extra knowledge. In my opinion, one can practice by gathering the least amount (often thought of as enough) of data to make a decision or one can gather as much as possible to minimize risk to the patient. In critical care regardless of location (ED, ICU, post op, in the OR etc.) we look for unicorns everyday. At least I do. How often… Read more »

Vote Up0Vote Down Reply

3 years ago

Guest

Derek Louey

Could you then argue that once the first gas has excluded a mixed disorder that you could confidently then use serum bicarbonate as the de facto marker to monitor the resolution of acidosis?

What it the likelihood of another unicorn that unexpectedly develops in the meantime e.g. saline acidosis?

Vote Up0Vote Down Reply

3 years ago

Guest

Craig Rosebrock MD

The issue with doing anything with confidence in the ICU relies on the patient going by the book frankly.

so I tend look at each patient as different. So I think that at times you can rely on the bicarbonate after the first gas…but you dont know which patient that is going to be

I am not trying to stir the pot…it is just how I practice.

I have tried the minimal type approach to medicine…did if for a few years out of fellowhip…ya know not getting daily films on vented folks or tying to give people lab holidays etc…you get burned in the end and the patient can suffer. People develop anemia for no apparent reason and gas exchange in ards can get worse fast with minimal changes in need of 02.

Vote Up0Vote Down Reply

3 years ago

Guest

Craig Rosebrock MD

I love the debates and discussions here but we have to keep in mind that when we say that we should abandon the abg or vbg on all patients WITH DKA we need to be careful of what outcomes this can have. I worry that somebody reading this with less clinical days in the field may just abandon the use all together. There is some merit to making the mistakes as you call them…one sees who needs the gas and who does not.

Ignore the fact that I work in the peds world….. we use either a VBG/ABG for placement ICU vs. Ward… then we start a protocol fluid set. We dose Humalog SQ, or an insulin gtt, then watch the POC glucose over the next 24 hours or so until they correct, and do teaching…

Agree, the precipitating factor and overall clinical context are the key prognostic factors. The patients with DKA who do poorly are usually patients with severe underlying illness which is triggering the DKA (often sepsis).

Vote Up0Vote Down Reply

3 years ago

Guest

Harry Frankfuter

Great discussion! Very forward thinking and progressive. My concern is that bicarbonate is not a perfect proxy for acid base status. You can have low bicarbonate and not have a low pH. Either because you have a mixed process or because you simply have lost bicarbonate through some independent mechanism. I think this is correlated to the quantitative approach to acid/base which says, a la Weingart, that bicarbonate is a dependent, not independent variable. Being acidotic causes your bicarb to be low. NOT that having low bicarb causes you to be acidotic. Therefore, you can’t say you’re acidotic just because you have a low bicarb. I think the bigger picture and you definitely hit upon this is whether your acid base status really matters. And this of course is really heretical stuff. The traditional teaching has always been when you get too acidotic your catecholamine receptors cease to function. Ok, but I don’t think that knowing the pH actually changes management. If your DKA patient is acidotic and therefore hypotensive, what do you do? You give fluids. If your DKA patient was hypotensive and you didn’t know their acid base status what would you do? Give fluids. However, the abg/vbg… Read more »

The anion gap is actually wonderful for the resolution of DKA, and primarily what we use. If you correct anion gap for ALB, it is identical to BD method (though Josh and I could debate whether you need to do this.) Just think of it as BD with the SID portion already taken out of the equation. BD eliminates respiratory acid/base leaving only metabolic. Anion Gap eliminate NAGMA portion of the BD leaving only unmeasured. Both BD and Anion Gap should be corrected with lactate, and B-HB if available.

The diagnostic criteria for DKA are very clear but what is not clear (as so often) is what to do when a patient meets some of these criteria, but not others. We have also seen DKA with a normal serum bicarb, or a normal pH, or no anion gap. If we are seeking maximum sensitivity, then we may want to say meeting any of those criteria makes you DKA, in which case you need the VBG to rule it out. On the other hand if we want more specificity we might say we want three or four of the criteria, +/- typical symptoms, in order to call it DKA. In that case you will rarely need a VBG to make the diagnosis. Not to complain, but a list of all the classic findings in DKA doesn’t help me much. Patients who have all of them, or none of them, aren’t challenging. They should really include some sort of a scoring system for cases (which are the rule) where some but not all of these features are present. For example, what about a diabetic patient with abdominal pain, a little vomiting, a glucose of >500, with a slightly depressed serum bicarb… Read more »

not to butt in here, but I am not seeing how you have DKA without an Anion gap and how a VBG would be helpful at that point, or why a VBG would ever be helpful over the Anion Gap. And in your example how you would be down 10 mmol of bicarb in a vomiting patient no less where there should be a hypochloremic alkalosis rather than a hyperchloremic acidosis.

Vote Up0Vote Down Reply

2 years ago

Guest

Dr. Rekha Sthapit, DM EM resident, TUTH, Nepal

Dear Dr. Josh,
thank you for the nice piece of information.It was an eye opener to me! Could you please be more specific what is meant by flooding with lot of NS in DKA, because as far as I know, we generally give fluids as per protocol in DKA.